GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 14 Mar 2013.
Ataxia telangiectasia mutated homolog
Atm
serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from
NCBI)
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Papers on
Atm
The loss of the BH3-only Bcl-2 family member Bid delays T-cell leukemogenesis in Atm-/- mice.
New
Nashville, United States. In Cell Death Differ, 08 Apr 2013
Loss of the ATM (ataxia telangiectasia mutated)-mediated DDR in mice results in T-cell leukemia driven by accumulation of DNA damage accrued during normal T-cell development.
ATM kinase activity modulates ITCH E3-ubiquitin ligase activity.
New
Roma, Italy. In Oncogene, 25 Mar 2013
Ataxia Telangiectasia Mutated (ATM) kinase, a central regulator of the DNA damage response, regulates the activity of several E3-ubiquitin ligases, and the ubiquitination-proteasome system is a consistent target of ATM.
T-cell-specific deletion of Mof blocks their differentiation and results in genomic instability in mice.
New
Dallas, United States. In Mutagenesis, 05 Mar 2013
Similarly, ataxia telangiectasia mutated (Atm)-deficient mice exhibit severe defects in T-cell maturation and eventually develop thymomas.
Essential Developmental, Genomic Stability, and Tumour Suppressor Functions of the Mouse Orthologue of hSSB1/NABP2.
New
Australia. In Plos Genet, 28 Feb 2013
We recently identified SSB1 as a novel protein critical for the initiation of ATM signaling and DNA double-strand break repair by homologous recombination.
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
New
Impact
Tokyo, Japan. In Nat Med, Aug 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
New
Impact
Singapore, Singapore. In Cell Metab, Aug 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Targeting p38 mitogen-activated protein kinase signaling restores subventricular zone neural stem cells and corrects neuromotor deficits in Atm knockout mouse.
New
United States. In Stem Cells Transl Med, Jul 2012
We have previously identified an oxidative stress-mediated increase in phospho-p38 mitogen-activated protein kinase (MAPK) and the resultant downregulation of Bmi-1 and upregulation of p21 as key components of the mechanism causing defective proliferation of neural stem cells (NSCs) isolated from the subventricular zone (SVZ) of Atm(-/-) mice.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
New
Impact
United States. In Nat Med, May 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
ATM controls meiotic double-strand-break formation.
Impact
New York City, United States. In Nature, 2011
Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair.
Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.
Review
Sioux Falls, United States. In Drug Discov Today, 2011
The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cell-cycle progression.
The RAG2 C terminus suppresses genomic instability and lymphomagenesis.
Impact
New York City, United States. In Nature, 2011
Defects in DNA damage response factors such as ataxia telangiectasia mutated (ATM) protein and combined deficiencies in classical non-homologous end joining and p53 predispose to RAG-initiated genomic rearrangements and lymphomagenesis.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Impact
GeneRIF
Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
Mdm2 links genotoxic stress and metabolism to p53.
Review
Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Review
Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
GeneRIF
Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
GeneRIF
Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
GeneRIF
London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
Phosphorylation of ATM by Cdk5 mediates DNA damage signalling and regulates neuronal death.
Impact
GeneRIF
Atlanta, United States. In Nat Cell Biol, 2009
Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.
Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?
Review
Göteborg, Sweden. In Mol Microbiol, 2008
In Schizosaccharomyces pombe, the Ataxia Telangiectasia-mutated (Atm)/Atm and Rad 3 Related (Atr) homologue Rad3 is an essential regulator of the response to DNA damage and stalled replication forks.
ATM activation and DNA damage response.
Review
Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.
